The University of Osaka · Medicine
Professor Hidetatsu Outani's research lab specializes in musculoskeletal oncology and bone metabolism, focusing on the molecular mechanisms of rare bone tumors such as clear cell sarcoma and chondroblastoma, as well as the long-term outcomes and complications of bone tumor treatments. The lab investigates drug response mechanisms, epigenetic regulation of fusion oncogenes like *EWSR1::ATF1*, and the pathogenesis of atypical femoral fractures associated with long-term bone-modifying agents. Their work integrates preclinical models, including cell lines and xenografts, to advance personalized therapeutic strategies and improve patient outcomes in bone sarcomas and metabolic bone disorders.
Figures are computed from collected data and may differ slightly.
CCS is a rare, devastating disease, and our established CCS cell line and xenograft model may be a useful tool for further in-depth investigation and understanding of the drug-sensitivity mechanism.
ECI autografts are a durable option for reconstruction after resection of musculoskeletal tumors and provide good function over more than 15 years. Most graft failures occurred within 5 years of the index surgery. However, composite grafts showed a tendency to fail more than 10 years after the surgery.
Tumor size and grade govern prognosis in surgically-treated localized SS in long-term settings. If adequately treated patients have not developed metastases for 5 years after surgery, the risk of subsequently developing metastases was lower than previously reported.
Curettage and SBS filling had been found to be a reasonable treatment method for CB, which commonly occurs in the epiphysis or apophysis. Radiographic joint degeneration was not uncommon after CB treatment, especially in the talus and proximal humerus.
This study reveals the epigenetic and transcriptional suppression mechanism of the fusion oncogene <i>EWSR1::ATF1</i> in clear cell sarcoma by histone deacetylase inhibitor treatment as well as identifying SOX10 as a transcription factor that regulates <i>EWSR1::ATF1</i> expression.
Atypical femoral fractures (AFFs) are recently observed as a complication of long-term bone-modifying agent (BMA; bisphosphonate or denosumab) therapy for bone metastases. We describe the cases of two women diagnosed with breast cancer who developed incomplete AFF associated with BMAs prescribed for bone metastases. Radiographs of their femurs revealed thickening of the lateral subtrochanteric cortex, and tomosynthesis revealed a visible fracture line in the thickened cortex. They were initially
Our case series suggests that patients with localised synovial sarcoma of the hand may have favourable outcomes. Wide excision or marginal excision, followed by radiation therapy combined with chemotherapy, represent acceptable treatment strategies for synovial sarcoma of the hand. Regional lymph node dissection does not seem to be essential for synovial sarcoma of the hand.
Outani, Hidetatsu MD, PhD; Akita, Hirofumi MD, PhD; Nakai, Takaaki MD, PhD; Takada, Ryoji MD; Imura, Yoshinori MD, PhD; Tanaka, Takaaki MD, PhD; Tamiya, Hironari MD, PhD; Oshima, Kazuya MD, PhD; Takahashi, Hidenori MD, PhD; Ohkawa, Kazuyoshi MD, PhD; Katayama, Kazuhiro MD, PhD; Araki, Nobuhito MD, PhD; Naka, Norifumi MD, PhDAuthor Information
Chondromyxoid fibroma is a rare benign tumor, which is composed of immature myxoid mesenchymal tissue with features of early primitive cartilaginous differentiation, accounting for less than 1% of all primary bone tumors. Chondromyxoid fibromas arising from the ilium are relatively rare. Reports on fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging for chondromyxoid fibroma are limited. We present a case of a chondromyxoid fibroma of the left ilium with fluorodeoxyglucose-positron
Synovial sarcoma (SS), a rare subtype of soft-tissue sarcoma distinguished by expression of the fusion gene SS18-SSX, predominantly affects the extremities of young patients. Existing anticancer drugs have limited efficacy against this malignancy, necessitating the development of innovative therapeutic approaches. Given the established role of SS18-SSX in epigenetic regulation, we focused on bromodomain and extra-terminal domain protein (BET) inhibitors and epigenetic agents. Our investigation o
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